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Can Beta-2-Adrenergic Pathway Be a New Target to Combat SARS-CoV-2 Hyperinflammatory Syndrome?-Lessons Learned From
Antonio Barbieri1, Nirmal Robinson2, Giuseppe Palma1
1Animal Facility, Istituto Nazionale Tumori, Istituto Di Ricovero e Cura a Carattere Scientifico "Fondazione G. Pascale", Naples, Italy.
Abstract:
SARS-CoV-2 infection is a new threat to global public health in the 21st century (2020), which has now rapidly spread around the globe causing severe pneumonia often linked to Acute Respiratory Distress Syndrome (ARDS) and hyperinflammatory syndrome. SARS-CoV-2 is highly contagious through saliva droplets. The structural analysis suggests that the virus enters human cells through the ligation of the spike protein to angiotensin-converting enzyme 2 (ACE2). The progression of Covid-19 has been divided into three main stages: stage I-viral response, stage II-pulmonary phase, and stage III-hyperinflammation phase. Once the patients enter stage III, it will likely need ventilation and it becomes difficult to manage. Thus, it will be of paramount importance to find therapies to prevent or slow down the progression of the disease toward stage III. The key event leading to hyperinflammation seems to be the activation of Th-17 immunity response and Cytokine storm. B2-adrenergic receptors (B2ARs) are expressed on airways and on all the immune cells such as macrophages, dendritic cells, B and T lymphocytes. Blocking (B2AR) has been proven, also in clinical settings, to reduce Th-17 response and negatively modulate inflammatory cytokines including IL-6 while increasing IFNγ. Non-selective beta-blockers are currently used to treat several diseases and have been proven to reduce stress-induced inflammation and reduce anxiety. For these reasons, we speculate that targeting B2AR in the early phase of Covid-19 might be beneficial to prevent hyperinflammation.
Insights
Targeting beta-2 adrenergic receptors (B2AR) early in COVID-19 may prevent hyperinflammation. Blocking B2AR could reduce inflammatory cytokines and Th-17 responses, potentially improving patient outcomes and preventing severe disease progression.
Area of Science:
- Immunology
- Virology
- Pharmacology
Background:
- COVID-19, caused by SARS-CoV-2, presents a significant global health challenge, leading to severe pneumonia, ARDS, and hyperinflammatory syndrome.
- The virus enters host cells via spike protein binding to ACE2, and disease progression involves distinct stages, with Stage III characterized by dangerous hyperinflammation.
- Hyperinflammation in COVID-19 is linked to Th-17 immune responses and cytokine storms, necessitating early therapeutic interventions.
Purpose of the Study:
- To explore the potential of targeting beta-2 adrenergic receptors (B2AR) as an early therapeutic strategy for COVID-19.
- To investigate whether blocking B2AR can mitigate the hyperinflammatory phase of COVID-19 by modulating immune responses.
Main Methods:
- Review of existing literature on SARS-CoV-2 pathogenesis, immune responses, and the role of B2AR.
- Analysis of the expression of B2AR on immune cells and their involvement in inflammatory pathways.
- Speculative hypothesis based on known effects of B2AR blockade on Th-17 responses and cytokine production.
Main Results:
- B2ARs are expressed on key immune cells, including macrophages, dendritic cells, B cells, and T lymphocytes.
- Blocking B2AR has been shown to reduce Th-17 responses and inflammatory cytokines like IL-6, while increasing IFN-gamma.
- Non-selective beta-blockers are clinically used and known to reduce inflammation and anxiety.
Conclusions:
- Targeting B2AR in the early stages of COVID-19 presents a promising strategy to prevent the progression to hyperinflammation.
- Modulating B2AR activity may offer a novel therapeutic approach to control cytokine storms and improve COVID-19 outcomes.
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